The difference in mouse IgG1 with respect to complement fixing capacities will be investigated using tryptic fingerprinting and sequencing of the isolated, affinity purified antidinitrophenyl antibodies of the two different varieties (complement fixing and non-complement fixing). These experiments will also be extended by culturing in vitro the two cell lines in the absence or presence of tunicamycin to inhibit glycosilation and see if differences in carbohydrate content exist or not between the IgG1 of the two cell lines (complement fixing and non-complement fixing). The genetics of the suppressive trait will be investigated in recombinant inbred strains of mice (BALB/c by SJL) obtained from Dr. Melvin Cohn's laboratory (Salk Institute) and the "Biozzi High and Low" lines of mice obtained from Dr. Biozzi (Institut Curie, Paris). The possible role of a class specific (IgE) helper T cell will be investigated in the recombinant inbred SJA9 mouse which does not secrete IgE antibody though they possess B cells synthesizing the IgE class. The role of the IgD molecule in switching especially of switching from IgM to the IgE class will be investigated by injection from birth on of a monoclonal anti-IgD antibody which is known to greatly suppress the presence of surface IgD molecules. The role of immunization by various routes and with different adjuvants will help to learn more about the importance of surface IgD in the switching from IgM to other classes. The idiotype associated with anti-phenylarsonate antibodies of A/J mice is particularly useful to investigate the switching of H chains. This crossreacting idiotype was identified on the Fab fragment of IgG antibodies, its presence on IgE antibodies will be investigated. These investigations are important because of the extensive background of information on regulation of this idiotype.